Atherosclerosis最新文献

{"title":"Association of lipoprotein(a) and diabetes in primary prevention of coronary heart disease: The Multi-Ethnic Study of Atherosclerosis (MESA)","authors":"Rishi Rikhi ,&nbsp;Amier Haidar ,&nbsp;Harpreet S. Bhatia ,&nbsp;Kent Beam ,&nbsp;James McParland ,&nbsp;Richard Kazibwe ,&nbsp;Parag Chevli ,&nbsp;Christopher L. Schaich ,&nbsp;Monika Sanghavi ,&nbsp;Michael D. Shapiro","doi":"10.1016/j.atherosclerosis.2025.119179","DOIUrl":"10.1016/j.atherosclerosis.2025.119179","url":null,"abstract":"<div><h3>Background and Aims</h3><div>Lipoprotein(a) [Lp(a)] and diabetes are both independently associated with cardiovascular disease. Studies demonstrate that elevated Lp(a) is associated with increased incidence of cardiovascular disease in those with and without diabetes. However, it is unclear if Lp(a) modifies the association of diabetes and coronary heart disease (CHD) in primary prevention.</div></div><div><h3>Methods</h3><div>The present analysis included 6668 participants from the Multi-Ethnic Study of Atherosclerosis, a community-based cohort without clinical cardiovascular disease at baseline. Participants were categorized as follows: group 1: Lp(a) &lt; 50 mg/dL without diabetes, group 2: Lp(a) ≥50 mg/dL without diabetes, group 3: Lp(a) &lt; 50 mg/dL with diabetes, and group 4: Lp(a) ≥50 mg/dL with diabetes. Survival analysis using Kaplan-Meier and multivariable Cox proportional hazard models were performed to assess the relationship between Lp(a), diabetes, and time to incident CHD.</div></div><div><h3>Results</h3><div>In a fully adjusted model, log[Lp(a)] and diabetes were both independently associated with CHD (HR: 1.10; 95 % CI: 1.01, 1.20) and (HR:1.65; 95 % CI: 1.31, 2.06), respectively. There was a significant multiplicative interaction between logLp(a) and diabetes (<em>p</em> = 0.033). Compared to the reference group (Lp(a) &lt; 50 mg/dL without diabetes), in a fully adjusted model, those with Lp(a) ≥50 mg/dL without diabetes (group 2) had increased risk of CHD (HR: 1.29; 95 % CI: 1.00, 1.65). Similarly, individuals with Lp(a) &lt; 50 mg/dL with diabetes (group 3) also had greater risk of CHD (HR: 1.52; 95 % CI: 1.16, 1.98). The highest risk for CHD were in those with Lp(a) ≥50 mg/dL with diabetes (group 4) (HR: 2.57; 95 % CI: 1.77, 3.72).</div></div><div><h3>Conclusion</h3><div>The results of this analysis suggest that Lp(a) may modify the association between diabetes and CHD or that diabetes may modify the association between Lp(a) and CHD in those without cardiovascular disease at baseline. Further research is needed to clarify underlying mechanisms between Lp(a), diabetes, and CHD.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"404 ","pages":"Article 119179"},"PeriodicalIF":4.9,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143748665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Apolipoprotein (a) production and clearance are associated with plasma IL-6 and IL-18 levels, dependent on ethnicity” [Atherosclerosis (2024) 391 117474]","authors":"Anouk G. Groenen ,&nbsp;Anastasiya Matveyenko ,&nbsp;Nelsa Matienzo ,&nbsp;Benedek Halmos ,&nbsp;Hanrui Zhang ,&nbsp;Marit Westerterp ,&nbsp;Gissette Reyes-Soffer","doi":"10.1016/j.atherosclerosis.2025.119165","DOIUrl":"10.1016/j.atherosclerosis.2025.119165","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119165"},"PeriodicalIF":4.9,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prior exposure to doxorubicin exacerbates atherosclerotic plaque formation in apolipoprotein-E-deficient mice on a high-fat diet","authors":"Matthias Bosman ,&nbsp;Dustin Krüger ,&nbsp;Lynn Roth ,&nbsp;Wim Martinet ,&nbsp;Guido R.Y. De Meyer ,&nbsp;Emeline M. Van Craenenbroeck ,&nbsp;Pieter-Jan Guns","doi":"10.1016/j.atherosclerosis.2025.119168","DOIUrl":"10.1016/j.atherosclerosis.2025.119168","url":null,"abstract":"<div><h3>Background and aims</h3><div>Epidemiological data suggest that anthracyclines, such as doxorubicin (DOX), promote atherosclerosis in cancer survivors. However, this has not been established experimentally so far. Here, we investigated whether DOX pre-exposure exacerbates atherosclerotic plaque formation (Study 1) as well as the impact of DOX on plaque progression (Study 2). Further, we evaluated the role of alpha-1-antichymotrypsin (Serpina3n) and thrombospondin-1 (Thbs1) in these plaques as we previously identified these proteins to be associated with DOX-induced cardiovascular disease.</div></div><div><h3>Methods</h3><div>In Study 1, DOX (4 mg/kg body weight/week) was administered for three weeks to apolipoprotein-E-deficient mice followed by a high-fat plaque-promoting diet for 8 weeks. In Study 2, mice were fed a high-fat diet for 17 weeks with DOX administered concomitantly from the third week of diet for three weeks. Plaque size and composition were assessed in the thoracic aorta, brachiocephalic artery and proximal ascending aorta.</div></div><div><h3>Results</h3><div>Prior DOX exposure increased plaque size along the aortic tree, regardless of sex. This was accompanied by enhanced cell death (increased TUNEL positivity) as well as elevated Serpina3n and Thbs1 in plaques of DOX-treated mice. DOX did not change total cholesterol, HDL and LDL plasma concentrations. Conversely, concomitant DOX exposure did not enhance plaque size nor affect overall plaque composition along the aortic tree, highlighting the importance of experimental design.</div></div><div><h3>Conclusions</h3><div>Early DOX exposure exacerbated plaque development in mice, providing first experimental evidence for anthracycline chemotherapy as a possible risk factor for atherosclerosis in cancer patients.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119168"},"PeriodicalIF":4.9,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143715162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of a novel nutraceutical combination on low-density lipoprotein cholesterol and other markers of cardiometabolic health in adults with hypercholesterolaemia: A randomised double-blind placebo-controlled trial","authors":"Welma Stonehouse ,&nbsp;Bianca Benassi-Evans ,&nbsp;Jennie Louise","doi":"10.1016/j.atherosclerosis.2025.119177","DOIUrl":"10.1016/j.atherosclerosis.2025.119177","url":null,"abstract":"<div><h3>Background and aim</h3><div>Clinical evidence exists for LDL-cholesterol lowering by plant sterols, bergamot extract and artichoke leaf extract individually but their effect when combined is unknown. This study investigated the effects of a novel nutraceutical combining plant sterols, bergamot extract, artichoke leaf extract and hydroxytyrosol (referred to as ‘Cholesterol Balance’), on serum LDL-cholesterol (primary outcome), other cardiometabolic and oxidative stress markers in adults with hypercholesterolaemia.</div></div><div><h3>Methods</h3><div>Healthy adults (n = 42, 18-&lt;66 years, body mass index [BMI] &gt;18.5-&lt;35 kg/m²), with mild hypercholesterolaemia (LDL-cholesterol ≥2.5-&lt;5 mmol/L) and low CVD risk participated in a 4-month double-blind randomised placebo-controlled trial. Participants consumed either 3 capsules/day Cholesterol Balance (providing 375 mg Bergavit40™, 150 mg Altilix™, 1.8 g phytosterols, and 50 mg of Hydrovas10™ daily) or placebo. Outcomes were assessed at baseline, 2- and 4-months.</div></div><div><h3>Results</h3><div>There was no evidence that Cholesterol Balance affected serum LDL-cholesterol compared to placebo (adjusted mean difference [95 % CI] at 4 months between treatments, −0.12 [-0.34, 0.11] mmol/L, <em>p</em> = 0.307). None of the secondary outcomes, including total cholesterol, HDL-cholesterol, triglycerides, non-HDL-cholesterol, total cholesterol:HDL-cholesterol ratio, apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB), ApoB:ApoA1 ratio, plasma oxidised LDL, serum malondialdehyde, HbA1c, blood pressure or safety markers showed a significant difference between groups.</div></div><div><h3>Conclusion</h3><div>While safe to consume, a nutraceutical containing plant sterols, bergamot extract, artichoke leaf extract and hydroxytyrosol did not show evidence of improving serum LDL-cholesterol, or any other lipid and oxidative stress markers in adults with mild hypercholesterolaemia. Further research is needed to determine if ingredients in the complex formulation interact or interfere with LDL-cholesterol lowering mechanisms.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119177"},"PeriodicalIF":4.9,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143697195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Achilles tendon thickness with lipid profile and carotid IMT in patients with familial hypercholesterolemia","authors":"Masahito Michikura ,&nbsp;Masatsune Ogura ,&nbsp;Mika Hori ,&nbsp;Kota Matsuki ,&nbsp;Hisashi Makino ,&nbsp;Shimpei Fujioka ,&nbsp;Daisuke Shishikura ,&nbsp;Masaaki Hoshiga ,&nbsp;Mariko Harada-Shiba","doi":"10.1016/j.atherosclerosis.2025.119173","DOIUrl":"10.1016/j.atherosclerosis.2025.119173","url":null,"abstract":"<div><h3>Background and aims</h3><div>Familial hypercholesterolemia (FH) is characterized by high levels of low-density lipoprotein cholesterol (LDL-C) and Achilles tendon (AT) thickening. AT thickness (ATT) is useful for diagnosing FH and assessing the risk of coronary artery disease (CAD). Nevertheless, the relationship between AT thickening and lipid profile is not clear. We investigated the association of ATT with lipid Profile and carotid IMT.</div></div><div><h3>Methods</h3><div>We included 450 patients with clinically diagnosed heterozygous FH. ATT was measured by ultrasonography.</div></div><div><h3>Results</h3><div>The rate of thickening increased for both AT and carotid-IMT according to age (<em>p</em> &lt; 0.001). In the teens, there was no carotid-IMT thickening, but 39 % of the subjects had a thickened AT. The thresholds of cumulative LDL-C values for AT and carotid-IMT thickening based on ROC curves were 9210 mg/dL∗years (AUC: 0.66, 95 % CI: 0.61–0.72) for ATT and 11,255 mg/dL∗years (AUC: 0.79, 95 % CI: 0.75–0.84) for carotid-IMT. For cumulative LDL-C levels ≥ median, untreated HDL-C level was lower in the AT thickened group than in the non-thickened group (AT thickened: 52 (43–63) mg/dL, non-thickened: 63 (52–72) mg/dL). There was a significant correlation between ATT and cumulative LDL-C (Male: R = 0.48 <em>p</em> &lt; 0.001, Female: R = 0.33 <em>p</em> &lt; 0.001).</div></div><div><h3>Conclusions</h3><div>We clarified that both cumulative exposure to LDL-C and untreated HDL-C levels were closely related to AT thickening. Our results show that in ultrasonographic assessment, ATT is more useful than carotid-IMT for predicting the degree of lipid deposition in tissues, especially in young adults.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119173"},"PeriodicalIF":4.9,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143734556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simvastatin ameliorates senescence-induced mitochondrial dysfunction in vascular smooth muscle cells","authors":"C. Rossi ,&nbsp;C. Macchi ,&nbsp;C. D'Alonzo ,&nbsp;M. Venturin ,&nbsp;M. Ruscica ,&nbsp;A. Corsini ,&nbsp;C. Battaglia ,&nbsp;S. Bellosta","doi":"10.1016/j.atherosclerosis.2025.119176","DOIUrl":"10.1016/j.atherosclerosis.2025.119176","url":null,"abstract":"<div><h3>Background and aims</h3><div>Senescence and mitochondrial dysfunction are two major indicators of aging. Mitochondria are potential drivers of aging phenotypes and dysfunctional mitochondria are associated with several age-related diseases. There is evidence that senescence induces changes in mitochondrial structure, dynamics, and function. Moreover, senescent vascular smooth muscle cells (VSMCs) are present in atherosclerotic plaques and contribute to their instability. The anti-atherosclerotic effects of simvastatin are well known, but recently other benefits, such as promoting mitochondrial quality and senostatic effects, have been hypothesized. We aimed to analyze simvastatin's senostatic effects in senescent VSMCs.</div></div><div><h3>Methods</h3><div>We established and characterized mitochondrial dysfunction in doxorubicin-induced senescent VSMCs (doxorubicin) or VSMCs serially passaged to induce replicative senescence (old).</div></div><div><h3>Results</h3><div>We observed in both senescent models few typical senescence markers such as altered cell morphology, cell cycle inhibitors, laminB1, an accumulation of dysfunctional mitochondria characterized by reduced mitochondrial membrane potential (MMP) and respiration, accumulation of reactive oxygen species (ROS), and an altered mitochondria morphology. Down-regulation of TFAM and TOM70 expression was observed only in old cells suggesting a reduction of mitochondrial biogenesis. Next, we investigated whether simvastatin could ameliorate age‐associated phenotypes in senescent VSMCs. Simvastatin 0.1 μM reduces the senescence-associated secretory phenotype (SASP) and ROS production and improves mitochondrial respiration in doxorubicin and old VSMCs. Interestingly, the effects of simvastatin on mitochondrial respiration and SASP were replicated by using a siRNA for the hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase, and abolished by adding mevalonic acid, suggesting that these effects are mediated through the inhibition of HMG-CoA reductase.</div></div><div><h3>Conclusions</h3><div>Our results suggest that simvastatin controls SASP and exerts potentially beneficial therapeutic effects by ameliorating senescence-induced mitochondrial dysfunction in senescent VSMCs.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119176"},"PeriodicalIF":4.9,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143715161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low-density lipoprotein-cholesterol subfractions as predictors for coronary artery calcium incidence and progression – The Brazilian longitudinal study of Adult Health (ELSA – Brasil)","authors":"Shamroz Farooq ,&nbsp;Giuliano Generoso ,&nbsp;Isabela M. Bensenor ,&nbsp;Raul D. Santos ,&nbsp;Steven R. Jones ,&nbsp;Eugenio Moraes ,&nbsp;Michael J. Blaha ,&nbsp;Peter P. Toth ,&nbsp;Paulo A. Lotufo ,&nbsp;Henrique L. Staniak ,&nbsp;Marcio S. Bittencourt","doi":"10.1016/j.atherosclerosis.2025.119171","DOIUrl":"10.1016/j.atherosclerosis.2025.119171","url":null,"abstract":"<div><h3>Background and aims</h3><div>Low-density lipoprotein-cholesterol (LDL-c) subfractions may play different roles in atherogenesis. Our objective was to evaluate the association between LDL-c subfractions and coronary artery calcium (CAC) incidence in individuals with a baseline CAC = 0 and CAC progression in those with CAC &gt; 0 at baseline.</div></div><div><h3>Methods</h3><div>We include 2632 participants from the Brazilian Longitudinal Study of Adult Health cohort, all of whom underwent two repeated CAC score measurements and had LDL-c subfraction measurements. The LDL-c subfraction concentrations were measured by the vertical auto profile method and categorized as small dense LDL-c (sdLDL-c) and large buoyant LDL-c (lbLDL-c). We constructed logistic regression analyses to examine CAC incidence and CAC progression. Additionally, CAC progression was analyzed using linear regression analyses as continuous variables.</div></div><div><h3>Results</h3><div>At baseline, a total of 2066 individuals (47.2 years, 62.2% female) had CAC = 0 and 566 (53.63 years, 36.9% female) had CAC &gt; 0. The mean interscan interval was (5.15 ± 2.37 years). We found a significant association between sdLDL-c and CAC incidence (OR, 1.29 [95% CI, 1.13–1.47]) but not for lbLDL-c (<em>p</em> = 0.28) after adjustment for confounders. We found no association of the sdLDL-c fraction with CAC progression in any of the analyses. However, lbLDL-c concentrations were inversely associated with CAC progression on both logistic and linear regression analyses (all <em>p</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>There is a positive association between incidence of CAC and sdLDL-c but not lbLDL-c. CAC progression was inversely associated with lbLDL-c but not with sdLDL-c.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119171"},"PeriodicalIF":4.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143704959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between statin adherence and arterial stiffness in young adult patients with familial hypercholesterolemia: A cross-sectional study","authors":"Sibbeliene E. van den Bosch ,&nbsp;Barbara A. Hutten ,&nbsp;Alma Revers ,&nbsp;Eric M. Schrauben ,&nbsp;Pim van Ooij ,&nbsp;Aart J. Nederveen ,&nbsp;Willemijn E. Corpeleijn ,&nbsp;Albert Wiegman","doi":"10.1016/j.atherosclerosis.2025.119175","DOIUrl":"10.1016/j.atherosclerosis.2025.119175","url":null,"abstract":"<div><h3>Background</h3><div>Familial hypercholesterolemia (FH) causes elevated low-density lipoprotein cholesterol (LDL-C) levels, leading to an increased risk for premature atherosclerotic cardiovascular disease (ASCVD). To prevent ASCVD, lipid-lowering therapy (LLT), such as statins, is needed from childhood on, to lower LDL-C levels. Arterial stiffness can serve as a surrogate marker for atherosclerosis. The aim of this study is to determine the association between statin adherence and arterial stiffness in young adults with FH.</div></div><div><h3>Methods</h3><div>The cohort for this cross-sectional study originally consisted of 214 children with heterozygous FH who participated in a placebo-controlled trial on the efficacy and safety of pravastatin, and all continued on LLT. After 20 years, these patients were invited for a follow-up visit, including a questionnaire where they reported the percentage of prescribed LLT they had taken over the past month, as well as a 4D flow MRI examination to assess carotid pulse wave velocity (PWV), in m/s.</div></div><div><h3>Results</h3><div>We included 134 patients with FH (mean (SD) age: 31.7 (3.2) years; 67 (50.0 %) males). A higher adherence (%) to statin therapy was significantly associated with lower PWV (beta [β] −0.003 (95 % confidence interval [CI] −0.007 to −0.000); <em>P</em> = 0.039)<strong>.</strong> After adjustment for potential confounders, this association remained similar (β −0.003 (95 % CI -0.007 to −0.000), <em>P</em> = 0.031).</div></div><div><h3>Conclusions</h3><div>The results of our study suggest that higher adherence to statin therapy is associated with less arterial stiffness, thereby reducing the risk for ASCVD compared to lower levels of adherence. These findings highlight the importance of adherence to LLT in patients with FH.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"404 ","pages":"Article 119175"},"PeriodicalIF":4.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143833254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The emerging role of glycans and the importance of sialylation in cardiovascular disease","authors":"Naomi E. Wattchow ,&nbsp;Benjamin J. Pullen ,&nbsp;Anuk D. Indraratna ,&nbsp;Victoria Nankivell ,&nbsp;Arun Everest-Dass ,&nbsp;Peter J. Psaltis ,&nbsp;Daniel Kolarich ,&nbsp;Stephen J. Nicholls ,&nbsp;Nicolle H. Packer ,&nbsp;Christina A. Bursill","doi":"10.1016/j.atherosclerosis.2025.119172","DOIUrl":"10.1016/j.atherosclerosis.2025.119172","url":null,"abstract":"<div><div>Glycosylation is the process by which glycans (i.e. ‘sugars’) are enzymatically attached to proteins or lipids to form glycoconjugates. Growing evidence points to glycosylation playing a central role in atherosclerosis. Glycosylation occurs in all human cells and post-translationally modifies many signalling molecules that regulate cardiovascular disease, affecting their binding and function. Glycoconjugates are present in abundance on the vascular endothelium and on circulating lipoproteins, both of which have well-established roles in atherosclerotic plaque development. Sialic acid is a major regulator of glycan function and therefore the process of sialylation, in which sialic acid is added to glycans, is likely to be entwined in any regulation of atherosclerosis. Glycans and sialylation regulators have the potential to present as new biomarkers that predict atherosclerotic disease or as targets for pharmacological intervention, as well as providing insights into novel cardiovascular mechanisms. Moreover, the asialoglycoprotein receptor 1 (ASGR1), a glycan receptor, is emerging as an exciting new regulator of lipid metabolism and coronary artery disease. This review summarises the latest advances in the growing body of evidence that supports an important role for glycosylation and sialylation in the regulation of atherosclerosis.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119172"},"PeriodicalIF":4.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ethnic variations in neutrophil count as predictors of prognosis following acute myocardial infarction","authors":"Matthew Sadler ,&nbsp;Antonio Cannata ,&nbsp;Sarah Mackie ,&nbsp;Rupavidhya Mondi Anandhakrishna ,&nbsp;Fulye Argunhan ,&nbsp;Emma Ferone ,&nbsp;Al-Agil Mohammad ,&nbsp;Jamila Salim ,&nbsp;Narun Tantichirasakul ,&nbsp;Mei Tung Lam ,&nbsp;Josel Ambon ,&nbsp;Aamir Shamsi ,&nbsp;Susan Piper ,&nbsp;Giorgio Napolitani ,&nbsp;Ajay M. Shah ,&nbsp;Theresa McDonagh ,&nbsp;Paul A. Scott ,&nbsp;Lynn Quek ,&nbsp;Daniel I. Bromage","doi":"10.1016/j.atherosclerosis.2025.119169","DOIUrl":"10.1016/j.atherosclerosis.2025.119169","url":null,"abstract":"<div><h3>Aims</h3><div>Elevated neutrophils are associated with a poor prognosis after acute myocardial infarction (AMI) but it is not known if ethnicity influences the association between neutrophil count and outcome. We aimed to describe the temporal dynamics of neutrophils after AMI, and assess the interaction between ethnicity, neutrophil count, and outcomes after AMI.</div></div><div><h3>Methods</h3><div>Consecutive patients presenting with AMI between 2016 and 2023 were divided into two groups according to their median neutrophil count. Ethnicity was dichotomised as white and other ethnic groups combined (referred to as ‘ethnic minorities’). The primary outcome was in-hospital mortality, with a secondary outcome of 60-day mortality.</div></div><div><h3>Results</h3><div>In our study of 3062 AMI patients (76 % white, 24 % from ethnic minority groups), we found that neutrophil counts rose early post AMI, which coincided with a nadir of the other cell groups. We identified a relative baseline neutropenia in ethnic minority individuals, compared to white individuals (6.85 vs 8.42 × 10⁹/L). We observed a significant, independent association between elevated neutrophils at baseline and the primary outcome of in-hospital mortality (OR 2.06, p &lt; 0.001) and secondary outcome of 60-day all-cause mortality (HR 1.08, p = 0.002). Sub-group analysis revealed a significant interaction between ethnicity and elevated neutrophils (p = 0.004), indicating that a comparable neutrophil count conferred an increased risk for ethnic minority patients for both outcomes.</div></div><div><h3>Conclusions</h3><div>We report ethnicity-specific leucocyte dynamics after AMI. Furthermore, neutrophil count is associated with a disproportionate risk in ethnic minority compared with white individuals. Understanding post-AMI inflammation and its interaction with ethnicity is essential in providing personalised prognostication and patient management.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"403 ","pages":"Article 119169"},"PeriodicalIF":4.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143715108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}